Mind and Brain

Over the past century or so, we've learned a lot about the mental processes
of producing, perceiving and learning language. This knowledge is detailed
and extensive, but in most cases, we do not know how these processes are
actually implemented in the brain. Over the same period, we've learned
a great deal about the localization of different linguistic abilities
in different regions of the brain, and also about how neural computation
works in general. However, our understanding of how the brain creates
and understands language remains relatively crude. One of today's great
scientific challenges is to integrate the results of these two different
kinds of investigation -- of the mind and of the brain -- with the goal
of bringing both to a deeper level of understanding.

As a concrete example of this mind/brain dichotomy, consider the following.
From literally thousands of studies, we know that word frequency has
a large effect on mental processing of both speech and text: in all sorts
of tasks commoner words are processed more quickly than rarer ones, other
things equal. However, we don't know for sure how this is implemented
in the brain. Is "neural knowledge" of more common words stored
in larger or more widespread chunks of brain tissue? Are the neural representations
of common words more widely or strongly connected? Are the resting activation
levels of their neural representations simply higher? Are they less efficiently
inhibited? Amazingly enough, there is no clear evidence about the relative
contributions of these four different different kinds of brain mechanisms
to the phenomenon of word frequency effects.

Again, psychological research tells us that there is also a strong recency
effect: in all sorts of tasks, words that we've heard or seen recently
are processed more quickly. Again, we don't know how the recency effect
arises in the brain, nor do we know whether the brain mechanisms underlying
the frequency and recency effects are the partly or entirely the same.
There is no lack of speculation on these questions, but we honestly just
don't know at this point.

This simple example is typical. Very little of what we know about mental
processing of speech and language can be translated with confidence into
talk about the brain. At the same time, very little of what we know about
the neurology of language can now be expressed coherently in terms of
what we know about mental processing of language. For example, one of
the most striking facts about the neurology of speech and language is
lateralization: the fact that the one of the two cerebral hemispheres,
usually the left one, plays a dominant role in many aspects of language-related
brain function. However, we learn about this only by probing brain function
directly -- looking at the symptoms of stroke or head trauma, injecting
an anesthetic into the right or left internal carotic artery, imaging
cerebral blood flow during the performance of certain language-related
tasks, etc. There is nothing obvious in the behavioral or cognitive exploration
of linguistic activity that connects to its cerebral lateralization (though
we'll see later that there are some interestly non-obvious ideas about
this!)

The relation between mind and brain in general is a active "frontier"
area of science, in which the potential for progress is very great. The
neural correlates of linguistic activity, and the linguistic meaning of
neural activity, are especially interesting topics. Reports of current
research in this area are often presented at Penn, for example in the
meetings of the IRCS/CCN
Brain and Language group.

Functional localization of speech and language

Over the past couple of hundred years, most of what we know about how
language is processed in the brain has come from studies of the functional
consequences of localized brain injury, due to stroke, head trauma or
localized degenerative disease. More recently, tools for "functional
imaging" of the brain, such as fMRI, PET, MEG and ERP, provide a
new sort of evidence about the localization of mental processing in undamaged
brains. All of these techniques have their limitations, and so far they
have mainly confirmed and refined earlier conceptions rather than revolutionizing
them. However, over the next few decades these techniques promise enormous
strides in understanding how the brain works in general, and in particular
how it creates and understands language.

An excellent and detailed survey for a lay audience of what sorts
of processing go on where in the brain, with some speculation about how
and why, can be found in William
H. Calvin and George A. Ojemann's CONVERSATIONS WITH NEIL'S BRAIN
. If you are curious (and most people find the topic fascinating), you
should spend some time reading either the on-line version or the published
version of this book.

The taxonomy of language-related neurological problems, or aphasia,
has been elaborated over the past decades. There are many named aphasic
syndromes with clear instructions for differential
diagnosis, and a plausible story about how these syndromes are linked
to localization of language functions in the brain, and to injuries to
various brain tissues. We'll return shortly to a more elaborated table
of aphasic syndromes, with connections to diagnostic patterns and likely
areas of brain damage, after looking in more detail at the two basic categories
of aphasia that were identified by two 19th-century researchers, Paul
Broca and Carl Wernicke.

Broca's Aphasia and Wernicke's Aphasia

As a National Institutes of Health information page says:

Broca's aphasia results from damage
to the front portion of the language dominant side of the brain. Wernicke's
aphasia results from damage to the back portion of the language dominant
side of the brain.

Aphasia means "partial or total loss of the ability to articulate ideas...
due to brain damage."

A note of caution: functional localization varies, sometimes considerably,
across individuals. Brain injury (most commonly caused by stroke) is usually
widespread enough to affect several different functional areas. Thus each
patient is individual both in terms of symptoms and in terms of the correlation
of symptoms to area of damage. Nevertheless, there are broad syndromes
of deficit-associated-with-local-damage, as described succinctly in the
NIH passage above, that are characterized as Broca's and Wernicke's aphasia.

Here is a somewhat more precise picture of the typical placement of Broca's
area and Wernicke's area relative to various landmarks of cortical anatomy
and physiology:

Broca's aphasia is sometimes called disfluent aphasia or agrammatic aphasia.
It is named after Pierre-Paul Broca (1824-1880), a French surgeon and
anthropologist who first described the syndrome and its association with
injuries to a specific region of the brain.

Agrammatism typically involves laboured speech, and a lack of use of
syntax in speech production and comprehension (although patients who present
with agrammatic production may not necessarily have agrammatic comprehension).

Examiner What happened at the ball?
They didn't get married at the ball.

M.E.No, um, no...I don't know.
Shoe, um found shoe...

Here is a more detailed picture of the motor strip, showing
what is sometimes called the motor homunculus, which is a
depiction of how motor functions are localized along the motor strip. The
portion adjacent to Broca's area controls the face and mouth.

In between the motor strip and Broca's area are the areas known as the
supplementary motor area (SMA) and the premotor cortex, which are said
to be involved in the generation of action sequences from memory that
fit into a precise timing plan All in all, it seems likely that Broca's
area is connected to serialization of coordinated action of the speech
organs. Why do certain syntactic abilities also seem to be localized there?
Perhaps a neural architecture evolved for creating and storing complex
motor plans has been pressed into service to create and store symbolic
rather than purely motoric structures. As Deacon (1991) writes:

Human language has effectively colonized
an alien brain in the course of the last two million years. Evolution
makes do with what it has at hand. The structures which language recruited
to its new tasks came to serve under protest, so to speak. They were previously
adapted for neural calculations in different realms and just happened
to exhibit enough overlap with the demands of language processing so as
to make "retraining" and "reorganization" minimally costly in terms of
some as yet unknown evolutionary accounting. Many of the structural peculiarities
of language, its quasi-universals, and the way that it is organized within
the brain no doubt reflect this preexisting scaffolding.

The second classical aphasic syndrome is named after the German neurologist
Carl Wernicke (1848-1905).

Wernicke's aphasia is sometimes called sensory aphasia
or fluent aphasia. The speech of a Wernicke's patient is
often a normally-intoned stream of grammatical markers, pronouns, prepositions,
articles and auxiliaries, with difficulty in recalling correct content
words, especially nouns (anomia). Words may be meaningless
neologisms (paraphasia).

The patient in the passage below is trying to describe a picture of a
child taking a cookie.

C.B. Uh, well this is the ... the /dodu/ of this.
This and this and this and this. These things going in there like that.
This is /sen/ things here. This one here, these two things here. And the
other one here, back in this one, this one /gesh/ look at this one.

Examiner Yeah, what's happening there?

C.B. I can't tell you what that is, but I know
what it is, but I don't now where it is. But I don't know what's under.
I know it's you couldn't say it's ... I couldn't say what it is. I couldn't
say what that is. This shu-- that should be right in here. That's very
bad in there. Anyway, this one here, and that, and that's it. This is
the getting in here and that's the getting around here, and that, and
that's it. This is getting in here and that's the getting around here,
this one and one with this one. And this one, and that's it, isn't it?
I don't know what else you'd want.

Wernicke's patients seem to suffer from much greater disorders of thought
than Broca's patients, who often seem able to reason much as before their
stroke, but are simply unable to express themselves fluently. However, their
non-fluency causes them much frustration, and they are said to be unhappier
than Wernicke's patients, who are often blissfully unaware that nothing
they say makes any sense at all, and whose higher-level thinking processes
are often as haphazard as their language is.

Wernicke's area is at the boundary of the temporal and parietal lobes,
near the parietal lobe association cortex, where cross-modality integration
is said performed, and is adjacent to the auditory association cortex
in the temporal lobe. Thus Wenicke's aphasia is sometimes called a "receptive"
aphasia, by distinction with the "production" aphasia of the motor-system-related
Broca's syndrome. However, as the above examples indicate, Wernicke's
patients show plenty of problems in producing coherent discourse. Even
if Wernicke's area originally served a receptive function, it has been
taken over by the linguistic system just as Broca's area has been.

To give you some sense of what the injuries involved in this aphasic
syndromes are like, here is a photo of the excised brain of a Wernicke's
patient:

Here is a set of tomographic pictures of a different Wernicke's syndrome
brain, showing a series of horizontal slices. The front of the head is
towards the top, and the dominant (left) side is on the right, so it is
as if we are looking at the brain from the bottom:

Here is a similar set of tomographic pictures of the brain of a Broca's
patient:

The main point of these pictures: in these cases, the area of damage
is rather large.

A more elaborated taxonomy

The table below shows the relationship of 8 named aphasic syndromes to
six general types of symptoms:

Fluent

Repetition

Comprehension

Naming

Right-side
hemiplegia

Sensory
deficits

Broca

no

poor

good

poor

yes

few

Wernicke

yes

poor

poor

poor

no

some

Conduction

yes

poor

good

poor

no

some

Global

no

poor

poor

poor

yes

yes

Transcortical
motor

no

good

good

poor

some

no

Transcortical
sensory

yes

good

poor

poor

some

yes

Transcortical
mixed

no

good

poor

poor

some

yes

Anomia

yes

good

good

poor

no

no

Conduction aphasia generally results from lesion of the white-matter
pathways that connect Wernicke's and Broca's areas, especially the arcuate
fasciculus.

Global aphasia results from lesions to both Wernicke's and Broca's areas
at once.

The motor and sensory variants of transcortical aphasia are produced
by lesions in areas around Broca's and Wernicke's areas, respectively.

There are other syndromes as well, such as "pure word deafness",
in which the patient can speak and write more or less normally, but is
not able to perceive speech, even though other auditory perception is
intact.

In actual clinical diagnosis, more elaborate batteries of tests are commonly
given in order to assess language function in more detail, and the detailed
locations of lesions can be found by MRI imaging.

Connecting mind and brain? the declarative/procedural model

We began this lecture by stressing the apparent dissociation between
the phenomena of "language in the mind" and the phenomena of
"language in the brain." We'll end it with a brief presentation
of an idea that ties the observations about brain localization of language
to many other aspects of brain function, and at the same time makes contact
with some of the most basic distinctions in the cognitive architecture
of language. This idea has been proposed by Michael
Ullman and his collaborators, under the name of the "declarative/procedural
model."

Others have proposed a distinction between declarative memories
and procedural memories. Declarative memory is memory for facts,
like the color of a peach; procedural memory is memory for skills, like
riding a bicycle. The declarative memory system is specialized for learning
and processing arbitrarily-related information, and is based in temporal
(and temporal/parietal) lobe structures. The procedural memory system
is specialized for non-conscious learning and control of motor and cognitive
skills, which involve chaining of events in time sequence, and is based
in frontal/basal-ganglia circuits. Building on this earlier distinction,
Ullman proposes that what we think of as lexical knowledge (the association
of meaning and sound for morphemes, irregular wordforms and fixed or idiomatic
phrases) is crucially linked with the declarative, temporal-lobe system,
while what we think of as grammatical knowledge (productive methods for
real-time sequencing of lexical elements) is crucially linked to the procedural,
frontal/basal-ganglia system.

Ullman argues that declarative and lexical memory both involve learning
arbitrary conceptual/semantic relations; that the knowledge involved is
explicit, i.e. relatively accessible to consciousness; and that they involve
lateral/inferior temporal-lobe structures for already-consolidated knowledge,
and medial temporal-lobe structures for new knowledge. By contrast, procedural
and grammatical memory both involve coordination of procedures in real
time and computation of sequential structures;the knowledge involved in
both tends to be implicit and encapsulated, so that it is relatively inaccessible
to consciousness examination and control; and both involve frontal and
basal ganglia structures in the dominant hemisphere.

We can see this as a detailed elaboration of the old observation that
Wenicke's area is adjacent to primary auditory cortex, in the direction
of visual cortex and cross-modal association areas, while Broca's area
is adjacent to the portion of the motor strip that controls the vocal
organs. The declarative/procedural
model is supported by a wide variety of interesting, specific and
sometimes unexpected evidence, coming from psycholinguistic studies, developmental
studies, neurological cases, functional imaging studies and neurophysiological
observations.